Re: Previous COVID-19 Infection 0% Effective In Preventing Reinfection By Variants

This is a hypothesis. Why can our immune system remember small pox for a li fe-time, but can forget a corona virus after six months?

Here's a hint. The small pox virus is single linear double stranded DNA ge nome 186 kilobase pairs, which is lot more stable than the RNA strand in th e corona viruses (which is proof read during reproduction, so it's more sta ble than the RNA strand in the flu virus).

Lots of infected people and reproducing lots of virus particles - the more reproduction goes on, the more opportunities for variation.

Reproduction with variation, edited by selection. Straight Darwinism.

There are a bunch of things going on you're unaware off. The most likely cu lprit is an poorly understood antiviral, ribavirin. It was certainly involv ed in treating the cancer patient in whom the B1.1.7 UK mutation originat ed, and believed and immediately suspected by many to be the cause. South Africa is a place loaded with serious viral disease and a tremendous amount of anti-viral therapeutics. Ribavirin is in wide use there as well. It is currently being seriously researched as a method of inducing what's c alled lethal mutatgenesis in a multitude of RNA viruses. This is not a new concept. I recall it undergoing animal studies over 20 years ago- not sure they were using ribavirin for that or not. U.S. urban centers are another place which are ripe for spawning more mutat ions. The mutations are unnatural and are no accident. The SARS-CoV-2 is not evolving to become more resistant. All it has to do i s mutate, and the likelihood of improved resistance comes free.

The virus doesn't "respond" to pressures. There is no action of the enviro nment that makes it mutate. Mutation is literally random changes to the ge nome that are then selected for survival by the environment. The nature no r the rate of mutation does not change from environmental factors. The onl y impact the environment has on the mutations is that when the rate of infe ction increases there are more opportunities for mutations, so mutations oc cur more frequently when the infection rate is higher.

That's the really sad thing about depending on the vaccine rather than cont rolling the pandemic. While we try to vaccinate everyone, the virus is mut ating and is likely to develop some level of resistance to the vaccine. Th ere may already be strains resistant to the vaccine. With such high levels of infection even if we knock out the main strain through vaccination, tha t may allow the less prolific, resistant strain to flourish and become the dominant strain. Then we have another year to wait for the next vaccine.

It would surprise me if there weren't.

Hmmm... I think you fail to understand a lot about immunology.

onment that makes it mutate. Mutation is literally random changes to the ge nome that are then selected for survival by the environment. The nature nor the rate of mutation does not change from environmental factors. The only impact the environment has on the mutations is that when the rate of infect ion increases there are more opportunities for mutations, so mutations occu r more frequently when the infection rate is higher.

ntrolling the pandemic. While we try to vaccinate everyone, the virus is mu tating and is likely to develop some level of resistance to the vaccine.

You've just made the mistake you complained about. The virus just mutates. Some of the mutation may make the virus unrcognisable by an immune system t hat has been provoked by a particular vaccine - not all immune systems are going to latch on to the same features of the protein that the vaccine intr oduced so different people could well have different reactions to the same strain of the virus, even if they were all vaccinated by the same vaccine.

vels of infection even if we knock out the main strain through vaccination, that may allow the less prolific, resistant strain to flourish and become the dominant strain. Then we have another year to wait for the next vaccine .

Probably less. The 2020 vaccine development sprint has show-cased a lot of innovations, and seen many of them tested in practice. The next round of de velopment could go a lot faster. We've now got better program for working o ut how proteins fold - which is something that people have been working on for a decade or so.

Me too. Every time the virus has reproduces, it has a chance to mutate. If there has been lot of virus reproduction, as there has to be be when there are 157,369 new cases per day, there have to be a lot of mutant strains aro und. Most of the mutations will be inconsequential, and most of the rest wi ll be lethal to the strain that carries them, but with enough mutations you are going to see a few that make the virus more effective.

Don't we all. It is horribly complicated, and you have to work hard to keep track of cause and effect.

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ironment that makes it mutate. Mutation is literally random changes to the genome that are then selected for survival by the environment. The nature n or the rate of mutation does not change from environmental factors. The onl y impact the environment has on the mutations is that when the rate of infe ction increases there are more opportunities for mutations, so mutations oc cur more frequently when the infection rate is higher.

controlling the pandemic. While we try to vaccinate everyone, the virus is mutating and is likely to develop some level of resistance to the vaccine.

. Some of the mutation may make the virus unrcognisable by an immune system that has been provoked by a particular vaccine - not all immune systems ar e going to latch on to the same features of the protein that the vaccine in troduced so different people could well have different reactions to the sam e strain of the virus, even if they were all vaccinated by the same vaccine .

Bill, sometimes you are such an idiot. You start off telling me I'm wrong and proceed to tell me why I am right.

evels of infection even if we knock out the main strain through vaccination , that may allow the less prolific, resistant strain to flourish and become the dominant strain. Then we have another year to wait for the next vaccin e.

f innovations, and seen many of them tested in practice. The next round of development could go a lot faster. We've now got better program for working out how proteins fold - which is something that people have been working o n for a decade or so.

Faster, yes. A "lot" faster, depends on your definition of "a lot". And t he key word is "could". Not a terribly relevant point really.

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f there has been lot of virus reproduction, as there has to be be when ther e are 157,369 new cases per day, there have to be a lot of mutant strains a round. Most of the mutations will be inconsequential, and most of the rest will be lethal to the strain that carries them, but with enough mutations y ou are going to see a few that make the virus more effective.

That's probably the worst part of letting the disease rage while we wait fo r the vaccine, the high rate of infection contributes to a high rate of mut ation which can really make the durn thing hard to fight.

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ep track of cause and effect.

All the COVID-19 viruses are dangerous and are easily transmissible. We as a whole are too stupid to do what we need to do. So we will be stuck with this thing for some time.

I found out I am eligible to receive the vaccine now. I just need to get o n the list and get the durn shot. Communication about this is pretty bad r ight now. I hope it goes better than the Obamacare signup did.

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n controlling the pandemic. While we try to vaccinate everyone, the virus i s mutating and is likely to develop some level of resistance to the vaccine .

es. Some of the mutation may make the virus unrcognisable by an immune syst em that has been provoked by a particular vaccine - not all immune systems are going to latch on to the same features of the protein that the vaccine introduced so different people could well have different reactions to the s ame strain of the virus, even if they were all vaccinated by the same vacci ne.

and proceed to tell me why I am right.

The idiot here is you. I was complaining that you were attributing intent t o a virus which is just a dumb mechanism, and when I explain why the dumb m echanics produce the result that you are complaining about, you think I am supporting your conclusion, rather than objecting to way you got to it.

The virus doesn't "develop resistance" to the vaccine. Those strains that h appen to change in a way that makes the vaccine less effective are more lik ely to survive, but there's no way the virus could know how it needed to ch ange.

keep track of cause and effect.

s a whole are too stupid to do what we need to do. So we will be stuck with this thing for some time.

on the list and get the durn shot. Communication about this is pretty bad r ight now. I hope it goes better than the Obamacare signup did.

Good luck with getting immunised. Australia is getting close to starting va ccinations, but nobody here is dying of Covid-19 at the moment, so there's no particular urgency. People working health care and quarantine are going to get the first jabs - they are the only people likely to get exposed to t he virus in Australia at the moment and nobody wants them to pass it on to other patients.

People like me who are merely more likely to die of the infection if we get it are definitely in line, but it isn't urgent - we aren't getting infecte d at the moment though that can change if the local quarantine has another drop-off. The last one stopped our family Christmas get-together.

Actually there are some drugs which do increase the RNA mutation rate. (and possibly implicated in the formation of the UK Kent strain)

But from a systems wide point of view the virus mutates randomly and the selection effects of the constraints are treatments and counter measures we use against it select for the fittest ones to go on and reproduce.

In shorthand the virus *is* responding to the environmental constraints that we impose upon it. And the number of permutations it can explore is scaling with the number of active cases. Anything that gives a new variant the slightest edge in reproducing more efficiently will be selected for once it gets out of patient zero and into the population.

There are no experts who believe that we can stop this now other than with an effective vaccine rolled out worldwide.

It is puzzling that it hasn't been identified yet. CDC asleep on the job?

I understand it a lot more than you do.

One of the ways to select for strains which are drug resistant is to apply an inadequate dosage to quite kill them and allow the survivors to migrate up a concentration gradient of the drug on a growing medium.

Antibiotics do not work on viruses but the same rules apply to using antibodies or other only partially effective antivirals against them.

th an effective vaccine rolled out worldwide.

Granting the dire performance of the US and the UK in containing the virus, and the fact that there are number of countries who have done just as badl y, they are probably right, but even the US and the UK should have been abl e to learn enough from the countries that have done better to make it even without vaccine.

The US doesn't seem to have ever done as much testing as it should, and gen ome checking is even more expensive. I'm sure that there are plenty of peop le in the US who would like to do more, but the Trump administration doesn' t seem to have liked to spend money in ways that it couldn't easily justify to average Trump supporter.

You certainly think you do.